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Related Experiment Video

Updated: Jul 17, 2026

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome
06:51

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Published on: July 28, 2023

Intestinal microcirculatory dysfunction during the development of experimental necrotizing enterocolitis.

Yoshiya Ito1, Sarah M Doelle, Jessica A Clark

  • 1Department of Cell Biology, University of Arizona, Tucson, AZ 85724, USA.

Pediatric Research
|January 24, 2007
PubMed
Summary

Necrotizing enterocolitis (NEC) in premature rats impairs intestinal microcirculation, reducing blood flow. Increased endothelin-1 (ET-1) responsiveness contributes to these microcirculatory disturbances, highlighting potential therapeutic targets.

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A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 2021

Area of Science:

  • Neonatal physiology
  • Gastrointestinal pathophysiology
  • Vascular biology

Background:

  • Necrotizing enterocolitis (NEC) is a severe gastrointestinal emergency in premature infants.
  • Intestinal microcirculatory dysfunction is a key factor in NEC pathogenesis.
  • The role of endothelin-1 (ET-1) in NEC-associated microcirculatory changes requires further investigation.

Purpose of the Study:

  • To investigate alterations in intestinal microcirculation during NEC development in a rat model.
  • To determine the impact of endothelin-1 (ET-1) on intestinal microcirculation in NEC.
  • To explore the relationship between ET-1 signaling and microcirculatory disturbances in NEC.

Main Methods:

  • A rat model of NEC was established using prematurely born, formula-fed pups exposed to asphyxia and cold stress.
  • In vivo microscopic examination of ileal microcirculation was performed at various time points post-birth.
  • Laser Doppler flowmetry assessed intestinal blood flow, and ET-1 mRNA and ETB receptor expression were quantified.

Main Results:

  • Nutritive microvascular perfusion and intestinal blood flow were significantly reduced in the NEC group compared to dam-fed controls.
  • ET-1 messenger RNA (mRNA) levels in the ileum were markedly increased in NEC.
  • Microvascular responsiveness to ET-1 was heightened in NEC, correlating with decreased ETB receptor expression.

Conclusions:

  • Microcirculatory dysfunction in the distal ileum is a significant contributor to NEC progression in neonatal rats.
  • Enhanced microvascular sensitivity to ET-1, potentially due to altered ETB receptor expression, plays a role in NEC-related microcirculatory disturbances.